Articles: brain-injuries.
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J. Nerv. Ment. Dis. · Oct 1998
Posttraumatic stress symptomatology after childhood traumatic brain injury.
The purpose of this study was to quantify and to identify predictors of posttraumatic stress disorder (PTSD) symptomatology after traumatic brain injury (TBI). Fifty children aged 6 to 14 years, hospitalized after TBI, were assessed soon after TBI regarding injury severity and preinjury psychiatric, socioeconomic, family functioning, and family psychiatric history status; neuroimaging was also analyzed. Psychiatric assessments were repeated 3, 6, 12, and 24 months after TBI. ⋯ The presence of an internalizing disorder at time of injury followed by greater injury severity were the most consistent predictors of PTSD symptomatology. It is apparent, therefore, that PTSD and subsyndromal posttraumatic stress disturbances occur despite neurogenic amnesia. These problems should be treated, particularly if symptoms persist beyond 3 months.
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Journal of neurotrauma · Oct 1998
Soluble adhesion molecules in CSF are increased in children with severe head injury.
Leukocyte-endothelial adhesion molecules, critical to the development of acute inflammation, are expressed in brain as part of the acute inflammatory response to traumatic brain injury (TBI). We measured the concentrations of the adhesion molecules P-selectin, ICAM-1, E-selectin, L-selectin, and VCAM-1 in ventricular cerebrospinal fluid (CSF) from children with severe TBI (Glasgow coma score < 8) and compared these findings with those from children with bacterial meningitis. ⋯ These results are consistent with a specific acute inflammatory component to TBI in children. Future studies of secondary injury mechanisms and therapy after TBI should assess on the roles of P-selectin and ICAM-1 in injury and repair processes in brain after TBI.
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Journal of neurosurgery · Oct 1998
Randomized Controlled Trial Multicenter Study Comparative Study Clinical TrialA multicenter trial on the efficacy of using tirilazad mesylate in cases of head injury.
The authors prospectively studied the efficacy of tirilazad mesylate, a novel aminosteroid, in humans with head injuries. ⋯ Striking problems with imbalance concerning basic prognostic variables were observed in spite of the large population studied. These imbalances concerned pretreatment hypotension, pretreatment hypoxia, and the incidence of epidural hematomas. In future trials of pharmacological therapy for severe head injury, serious consideration must be given to alternative randomization strategies. Given the heterogeneous nature of head injury and the identification of populations that do relatively well with standard therapy, target populations with a higher risk for mortality and morbidity may be more suitable for clinical trials of such agents.
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Journal of neurotrauma · Oct 1998
Traumatic brain injury in the developing rat: effects of maturation on Morris water maze acquisition.
Previous work has demonstrated that postnatal and adult rats show different physiological responses to lateral fluid percussion (FP) brain injury. Compared to adult animals, the younger rats showed longer apnea and shorter unconsciousness, and sustained hypotension at all injury severities, with higher mortality following severe traumatic brain injury (TBI). To determine if these younger rats exhibit differential cognitive impairments, the Morris water maze (MWM) was used to compare the degree of spatial learning deficits between moderately injured postnatal day 17 (P17), P28, and adult rats, as well as their age-matched controls. ⋯ Injured P28s exhibited escape latency deficits during the first week, with 23% more trials to criterion and 24% fewer direct paths compared to P28 shams. In contrast, injured P17 rats showed no significant difference from age-matched controls in terms of escape latency, number of direct paths taken, or time to criterion performance. This work suggests that, upon surviving the insult, P17 injured rats show remarkable sparing compared to P28 and adult injured animals.
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Journal of neurotrauma · Oct 1998
ReviewNovel pharmacologic strategies in the treatment of experimental traumatic brain injury: 1998.
The mechanisms underlying secondary or delayed cell death following traumatic brain injury are poorly understood. Recent evidence from experimental models suggests that widespread neuronal loss is progressive and continues in selectively vulnerable brain regions for months to years after the initial insult. ⋯ This new knowledge has stimulated the development of novel therapeutic agents designed to modify gene expression, synthesis, release, receptor or functional activity of these pathological factors with subsequent attenuation of cellular damage and improvement in behavioral function. This article represents a compendium of recent studies suggesting that modification of post-traumatic neurochemical and cellular events with targeted pharmacotherapy can promote functional recovery following traumatic injury to the central nervous system.